Main Key Notes on Plastic Surgery

Key Notes on Plastic Surgery

,
0 / 0
How much do you like this book?
What’s the quality of the file?
Download the book for quality assessment
What’s the quality of the downloaded files?

This is the new edition of the concise but comprehensive handbook that should be owned by all surgical trainees specialising in plastic surgery. Taking a pithy systematic approach, Key Notes on Plastic Surgery offers the latest developments within the field in bullet point form and includes key papers for viva voces. It is informed by the current FRCS (Plast) curriculum, making it ideal preparation for the UK exit examination or equivalent international board exam.

 

Key features

  • Fully covers the entire scope of plastic surgery
  • Clearly divided into 10 sections with logical subheadings for easy fact-finding
  • Acts as an adjunct to the established longer texts
  • Brand new chapter on ethics and the law – a compulsory component of the oral examination
  • Illustrations outlining key surgical procedures and relevant anatomy

 

Fully revised to include all the latest clinical guidelines, Key Notes on Plastic Surgery is the perfect rapid reference tool for trainees in plastic surgery and dermatologic surgery who require quick, accurate answers.

Year:
2014
Edition:
2
Publisher:
Wiley-Blackwell
Language:
english
Pages:
640 / 641
ISBN 10:
1444334344
ISBN 13:
9781444334340
File:
PDF, 5.54 MB
Download (pdf, 5.54 MB)

You may be interested in Powered by Rec2Me

 

Most frequently terms

 
0 comments
 

You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you've read. Whether you've loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them.
1

Anfibios y reptiles

Año:
2004
Idioma:
spanish
Archivo:
PDF, 27,89 MB
0 / 0
2

Algebra II

Año:
1973
Idioma:
spanish
Archivo:
PDF, 28,00 MB
0 / 0
Key Notes on
Plastic Surgery
Adrian Richards
MBBS, MSc, FRCS (Plast)
Plastic and Cosmetic Surgeon
Aurora Clinics
Princes Risborough
UK

Hywel Dafydd
MB BChir, MA, MSc, FRCS (Plast)
Specialty Registrar
The Welsh Centre for Burns and Plastic Surgery
Morriston Hospital
Swansea
UK

SECOND EDITION

F O R E W O R D B Y P R O F E S S O R F U-C H A N W E I

This edition first published 2015
© 2015 by John Wiley & Sons, Ltd
© 2002 by Blackwell Science Ltd
Registered office:

John Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex,
PO19 8SQ, UK

Editorial offices:

9600 Garsington Road, Oxford, OX4 2DQ, UK
The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK
111 River Street, Hoboken, NJ 07030-5774, USA

For details of our global editorial offices, for customer services and for information about how to apply
for permission to reuse the copyright material in this book please see our website at
www.wiley.com/wiley-blackwell
The right of the author to be identified as the author of this work has been asserted in accordance with
the UK Copyright, Designs and Patents Act 1988.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or
transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or
otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior
permission of the publisher.
Designations used by companies to distinguish their products are often claimed as trademarks. All brand
names and product names used in this book are trade names, service marks, trademarks or registered
trademarks of their respective owners. The publisher is not associated with any product or vendor
mentioned in this book. It is sold on the understanding that the publisher is not engaged in rendering
professional services. If professional advice or other expert assistance is required, the services of a
competent professional should be sought.
The contents of this work are intended to further gener; al scientific research, understanding, and
discussion only and are not intended and should not be relied upon as recommending or promoting a
specific method, diagnosis, or treatment by health science practitioners for any particular patient. The
publisher and the author make no representations or warranties with respect to the accuracy or
completeness of the contents of this work and specifically disclaim all warranties, including without
limitation any implied warranties of fitness for a particular purpose. In view of ongoing research,
equipment modifications, changes in governmental regulations, and the constant flow of information
relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the
information provided in the package insert or instructions for each medicine, equipment, or device for,
among other things, any changes in the instructions or indication of usage and for added warnings and
precautions. Readers should consult with a specialist where appropriate. The fact that an organization or
Website is referred to in this work as a citation and/or a potential source of further information does not
mean that the author or the publisher endorses the information the organization or Website may
provide or recommendations it may make. Further, readers should be aware that Internet Websites
listed in this work may have changed or disappeared between when this work was written and when it
is read. No warranty may be created or extended by any promotional statements for this work. Neither
the publisher nor the author shall be liable for any damages arising herefrom.
Library of Congress Cataloging-in-Publication Data
Richards, Adrian M., author.
Key notes on plastic surgery / Adrian Richards, Hywel Dafydd ; foreword by professor Fu-Chan Wei. –
Second edition.
1 online resource.
Includes bibliographical references and index.
Description based on print version record and CIP data provided by publisher; resource not viewed.
ISBN 978-1-118-75686-7 (Adobe PDF) – ISBN 978-1-118-75699-7 (ePub) – ISBN 978-1-4443-3434-0
(pbk.)
I. Dafydd, Hywel, author. II. Title.
[DNLM: 1. Surgery, Plastic. WO 600]
RD119
617.9′ 52 – dc23
2014033321
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may
not be available in electronic books.
Cover image: © iStock.com/youngvet
Cover design by Andy Meaden
Set in 9.5/12pt Meridien by Laserwords Private Limited, Chennai, India
1

2015

Contents

Foreword

iv

Preface

v

Dedications

vi

Acknowledgements

vi

Abbreviations

vii

1

General Principles

2

Skin and Soft Tissue Lesions

3

The Head and Neck

133

4

The Breast and Chest Wall

264

5

The Upper Limb

309

6

The Lower Limb

422

7

The Trunk and Urogenital System

459

8

Burns

490

9

Aesthetic Surgery

530

Ethics, the Law and Statistics

591

Index

605

10

1
80

iii

Foreword

This second edition of Key Notes on Plastic Surgery distills the breadth and depth of the entire
specialty into a compact format. Clear, concise, accurate and accessible – that is what the
trainee desires when refreshing their memory of conditions during clinic, of reconstructive
algorithms before operating, and of the entire syllabus when preparing for plastic surgery
board examinations. Key Notes on Plastic Surgery fulfils this niche admirably.
A consistent balance has been struck between prose and bullet points throughout the book.
Key Notes on Plastic Surgery fosters understanding, facilitates the commitment of information
to memory, and provides structure to ease the recall of facts and principles. One can rapidly
glean key information with a glance at the page and yet solidify an understanding with a few
minutes’ read. The textual formatting and presentation of information is where this book
particularly shines.
Key Notes on Plastic Surgery will be embraced as a trusted companion by trainees all over the
world as they progress through training and sit for their board examinations. And when they
become established plastic surgeons, Key Notes on Plastic Surgery will take pride of place on
their bookshelves as a reliable quick reference handbook for teaching the next generation.
I highly recommend Key Notes on Plastic Surgery to all aspiring, training and established
plastic surgeons worldwide.
Fu-Chan Wei, MD, FACS
Distinguished Chair Professor
Chang Gung University
Medical College
Taipei, Taiwan
Academician
Academia Sinica
Taiwan

iv

Preface

Hywel Dafydd has updated and improved the first edition of Key Notes on Plastic Surgery.
He has worked tirelessly to include new and better diagrams and improve the content whilst
maintaining the book’s ethos – to succinctly communicate the essentials of Plastic Surgery.
We hope you enjoy the book and find it helpful in making you a better Plastic Surgeon.
Adrian Richards

The first edition of Key Notes has proved to be exceptionally popular for over a decade. Accessible, informative and succinct, it became the preferred handbook for innumerable plastic
surgery trainees. It was typeset with enough ‘white space’ to accommodate trainees’ notes
and sketches as they approached their final plastic surgery examination.
Nevertheless, an update was much-needed: the field of plastic surgery has moved on apace
and a detailed British plastic surgery syllabus was introduced. The material of the first edition has been updated, rewritten and expanded with several new sections to reflect this. In
addition, a new chapter is provided: ‘Ethics and the law’. The number of diagrams has more
than doubled, which should help with learning the ‘essentials’, such as cleft lip repair and
eyelid anatomy. Key Notes is now more complete and, although necessarily larger, remains
true to the format and style of the first edition. We hope that Key Notes continues to be useful
to plastic surgeons worldwide.
Hywel Dafydd

v

Dedications
AR – To my Family, Helena, Josie, Ciara, Alfie and Ned.
HD – For Jenny and Ioan.

Acknowledgements
As any Plastic Surgeon will tell you, the training and practice of the speciality takes dedication
and hard work. Writing a book in your free time adds to this and requires patience and
support from your family. For this reason I would like to thank my family Helena, Josie,
Ciara, Alfie and Ned for their constant support. I would also like to thank my surgical mentors
of whom there were many – in particular Brent Tanner and Michael Klaassen.
Adrian Richards

I would like to thank my wife Jenny and my son Ioan for their love and patience. Jenny also
helped edit final drafts for brevity. Thank you Per Hall for inspiring me to become a plastic
surgeon. Thanks to those who have trained me over the years in Cambridge, Wellington,
Leicester, Birmingham, Coventry, Swansea, Taipei, and Auckland. Special thanks to Sarah
Hemington-Gorse, Ian Josty, Dai Nguyen, Nick Wilson Jones, Tom Potokar, Peter Drew,
Leong Hiew, Hamish Laing, Dean Boyce, Max Murison and Ian Pallister, who spent hours
proofreading early drafts. I am also grateful to Rhidian Dafydd LLB, Karen Wong and Chris
Wallace, who checked much of the text for accuracy. Tom Macleod has been a constant
source of support and encouragement, and did a great deal of preparatory work on many
of the chapters. The book could not have been written without the staff of Morriston Hospital’s library. They sourced over 600 references from three centuries without as much as a
grumble: thank you Anne, Sue, Rita and Lisa.
Hywel Dafydd

vi

Abbreviations

5-FU
ABC
ABPI
AC
ACPA
ACR
ADH
ADM
ADM
AER
AFX
AICAP
AIDS
AIN
AJCC
AK
ALCL
ALH
ALS
ALT
ANOVA
AO
AP
APB
APC
APL
APR
APTT
ARDS
ASIS
ASSH
ATG
ATLS
AVA
AVM
AVN
BAAPS
BAHA

5-fluorouracil
Acinetobacter baumanii-calcoaceticus
ankle brachial pressure index
alternating current
anti-citrullinated protein antibody
American College of Rheumatology
atypical ductal hyperplasia
abductor digiti minimi
acellular dermal matrix
apical ectodermal ridge
atypical fibroxanthoma
anterior intercostal artery perforator (flap)
acquired immune deficiency syndrome
anal intraepithelial neoplasia
American Joint Committee on Cancer
actinic keratosis
anaplastic large T-cell lymphoma
atypical lobular hyperplasia
anti-lymphocyte serum
anterolateral thigh (flap)
analysis of variance
Arbeitsgemeinschaft für Osteosynthesefragen
anteroposterior
abductor pollicis brevis
antigen presenting cell
abductor pollicis longus
abdomino-perineal resection
activated partial thromboplastin time
adult respiratory distress syndrome
anterior superior iliac spine
American Society for Surgery of the Hand
anti-thymoglobulin
Advanced Trauma Life Support
arteriovenous anastomosis
arteriovenous malformation
avascular necrosis
British Association of Aesthetic Plastic Surgeons
bone-anchored hearing aid

vii

viii

Abbreviations

BAPRAS
BAPS
BCC
BDD
BEAM
BMI
BMP
BOA
BPD
BRAF
BRBN
BSA
BSSH
BXO
cAMP
CCNE
CEA
CFNG
CI
CIN
CL
CM
CMCJ
CMN
CNS
CO
COX
CP
CPAP
CPR
CRP
CRPS
CSAG
CSF
CT
CTA
CTLA
CTS
CVP
CVS
DASH
DBD
DC
DCIA

British Association of Plastic, Reconstructive and Aesthetic Surgeons
British Association of Plastic Surgeons
basal cell carcinoma
body dysmorphic disorder
bulbar elongation and anastomotic meatoplasty
body mass index
bone morphogenetic protein
British Orthopaedic Association
biliopancreatic diversion
B-Raf serine/threonine-protein kinase
blue rubber bleb naevus (syndrome)
body surface area
British Society for Surgery of the Hand
balanitis xerotica obliterans
cyclic adenosine monophosphate
Comité Consultatif National d’Ethique
cultured epithelial autograft
cross facial nerve grafting
cranial index
cervical intraepithelial neoplasia
cleft lip
capillary malformation
carpometacarpal joint
congenital melanocytic naevus
central nervous system
carbon monoxide
cyclooxygenase
cleft palate
continuous positive airways pressure
cardiopulmonary resuscitation
C-reactive protein
complex regional pain syndrome
Clinical Standards Advisory Group
cerebrospinal fluid
computed tomography
composite tissue allotransplantation
cytotoxic T-lymphocyte antigen
carpal tunnel syndrome
central venous pressure
cardiovascular system
Disabilities of the Arm, Shoulder and Hand
dermolytic bullous dermatitis
direct current
deep circumflex iliac artery

Abbreviations

DCIS
DD
DEXA
DFAP
DFSP
DICAP
DIEA
DIEP
DIPJ
DIY
DMARD
DNA
DOPA
DOT
DRUJ
DTH
EAST
EBV
ECG
ECRB
ECRL
ECU
EDC
EDM
EGF
EIP
ELND
EEMG
ELD
EMG
EMLA
ENT
EO
EPB
EPL
EPUAP
ER
ERK
ESBL
ESR
EULAR
FAMM
FAMM
FBC

ductal carcinoma in situ
Dupuytren’s disease
dual-energy X-ray absorptiometry
deep femoral artery perforator (flap)
dermatofibrosarcoma protuberans
dorsal intercostal artery perforator (flap)
deep inferior epigastric artery
deep inferior epigastric perforator (flap)
distal interphalangeal joint
do it yourself
disease-modifying antirheumatic drug
deoxyribonucleic acid
dihydroxyphenylalanine
double-opposing tab
distal radio-ulnar joint
delayed type hypersensitivity
elevated arm stress test
Epstein-Barr virus
electrocardiogram
extensor carpi radialis brevis
extensor carpi radialis longus
extensor carpi ulnaris
extensor digitorum communis
extensor digiti minimi
epidermal growth factor
extensor indicis proprius
elective lymph node dissection
evoked electromyography
extended latissimus dorsi (flap)
electromyography
eutetic mixture of local anaesthetic
ear, nose and throat
external oblique
extensor pollicis brevis
extensor pollicis longus
European Pressure Ulcer Advisory Panel
oestrogen receptor
extracellular-signal-regulated kinase
extended-spectrum beta-lactamase
erythrocyte sedimentation rate
European League Against Rheumatism
facial artery musculomucosal (flap)
familial atypical mole and melanoma (syndrome)
full blood count

ix

x

Abbreviations

FCR
FCU
FDA
FDG
FDM
FDMA
FDP
FDS
FFMT
FFP
FGF
FGFR
FIESTA
FISH
FLAIR
FNA
FNAC
FPB
FPL
GAG
GAS
GCS
GI
GLUT1
GMC
GP
Hb
HER
HES
HF
HFS
HIT
HIV
HLA
HMB-45
hMLH1
hMSH2
HPV
HRT
HTA
HU
ICAP
ICD
ICG

flexor carpi radialis
flexor carpi ulnaris
Food and Drug Administration
fluorodeoxyglucose
flexor digiti minimi
first dorsal metacarpal artery (flap)
flexor digitorum profundus
flexor digitorum superficialis
free functioning muscle transfer
fresh frozen plasma
fibroblast growth factor
fibroblast growth factor receptor
fast imaging employing steady-state acquisition
fluorescence in situ hybridisation
fluid attenuated inversion recovery
fine needle aspiration
fine needle aspiration cytology
flexor pollicis brevis
flexor pollicis longus
glycosaminoglycan
group A Streptococcus
Glasgow coma scale
gastro-intestinal
glucose transporter 1
General Medical Council
general practitioner
haemoglobin
human epidermal growth factor receptor
hydroxyethyl starch
hydrofluoric acid
Hannover Fracture Scale
heparin-induced thrombocytopenia
human immunodeficiency virus
human leukocyte antigen
human melanoma black 45
human mutL homolog 1 (gene)
human mutS homolog 2 (gene)
human papilloma virus
hormone replacement therapy
Human Tissue Authority
Hounsfield units
intercostal artery perforator (flap)
intercanthal distance
indocyanine green

Abbreviations

ICP
ICU
IDDM
IFN
IFSSH
IGA
IGAM
IGAP
IHC
IJV
IL
IMF
IMF
IMNAS
INR
IO
IOD
IPJ
IPL
IRG
ISSVA
ITL
ITU
IV
IVF
KA
KTP
KTS
LA
LASER
LCIS
LD
LDH
LDMF
LEAP
LHRH
LICAP
LISN
LM
LM
LME
LMM
LMWH
LRTI

intracranial pressure
intensive care unit
insulin dependent diabetes mellitus
interferon
International Federation of Societies for Surgery of the Hand
inferior gluteal artery
inferior gluteal artery myocutaneous (flap)
inferior gluteal artery perforator (flap)
immunohistochemistry
internal jugular vein
interleukin
inframammary fold
intermaxillary fixation
Institute of Medicine of the National Academy of Science
international normalised ratio
internal oblique
interorbital distance
interphalangeal joint
intense pulsed light
Independent Review Group
International Society for the Study of Vascular Anomalies
inferior temporal line
intensive therapy unit
intravenous
in vitro fertilisation
keratoacanthoma
potassium titanyl phosphate
Klippel-Trénaunay syndrome
local anaesthesia
light amplification by stimulated emission of radiation
lobular carcinoma in situ
latissimus dorsi
lactate dehydrogenase
latissimus dorsi miniflap
Lower Extremity Assessment Project
luteinising hormone releasing hormone
lateral intercostal artery perforator (flap)
lobular in situ neoplasia
lentigo maligna
lymphatic malformation
line of maximum extensibility
lentigo maligna melanoma
low-molecular-weight heparin
ligament reconstruction and tendon interposition

xi

xii

Abbreviations

LSI
LSMDT
MACS
MAGPI
MAL
MAPK
MARIA
MART
MCA
MCC
MCPJ
MDT
MEK
MESS
MFH
MHC
MHRA
MIP
MLD
MM
MMF
MODS
MPNST
MRC
MRI
MRKH
MRND
MRSA
MS
MSG
MSH
MSLT
MSU
MSX2
mTOR
MTPJ
MTT
NAC
NAI
NASHA
NCS
NF
NG
NHS

Limb Salvage Index
local skin cancer multidisciplinary team
Minimal Access Cranial Suspension
meatal advancement and glanuloplasty incorporated
methyl aminolevulinate
mitogen-activated protein kinase
Multistatic Array Processing for Radiowave Image Acquisition
melanoma antigen recognised by T cells
Mental Capacity Act
Merkel cell carcinoma
metacarpophalangeal joint
multidisciplinary team
mitogen/extracellular signal-regulated kinase
Mangled Extremity Severity Score
malignant fibrous histiocytoma
major histocompatibility complex
Medicines and Healthcare Products Regulatory Agency
megameatus intact prepuce
manual lymphatic drainage
malignant melanoma
mandibulomaxillary fixation
multiple organ dysfunction syndrome
malignant peripheral nerve sheath tumour
Medical Research Council
magnetic resonance imaging
Mayer–Rokitansky–Küster–Hauser (syndrome)
modified radical neck dissection
methicillin resistant Staphylococcus aureus
muscle sparing
Melanoma Study Group
melanocyte-stimulating hormone
Multicenter Selective Lymphadenectomy Trial
monosodium urate
msh homeobox 2 (gene)
mammalian target of rapamycin
metatarsophalangeal joint
malignant triton tumour
nipple-areola complex
non-accidental injury
non-animal stabilised hyaluronic acid
nerve conduction studies
neurofibromatosis
nasogastric
National Health Service

Abbreviations

NICH
NK
NOE
NPA
NPI
NPUAP
NPWT
NSAID
NSM
NVB
OA
OGS
OM
OP
ORIF
PA
PAL
PABA
PAF
PCNA
PDE
PDE
PDGF
PDS
PDT
PEEP
PET
PET
PHA
PIN
PIP
PIPJ
PL
PL
PMMA
PMN
POSI
PR
PRPC
PRS
PSI
PSIS
PT
PT

noninvoluting congenital haemangioma
natural killer (cell)
nasoorbitoethmoidal
nasopharyngeal airway
Nottingham Prognostic Index
National Pressure Ulcer Advisory Panel
negative pressure wound therapy
non-steroidal anti-inflammatory drug
nipple sparing mastectomy
neurovascular bundle
osteoarthritis
orthognathic surgery
osteomyelitis
opponens pollicis
open reduction and internal fixation
posteroanterior
power-assisted liposuction
para-amino benzoic acid
platelet activating factor
proliferating cell nuclear antigen (gene)
phosphodiesterase
Photodynamic Eye
platelet-derived growth factor
polydioxanone sulphate
photodynamic therapy
positive end-expiratory pressure
polyethylene terephthalate
positron emission tomography
progressive hemifacial atrophy
posterior interosseous nerve
Poly Implant Prothèse
proximal interphalangeal joint
palmaris longus
phospholipid
polymethylmethacrylate
polymorphonuclear neutrophils
position of safe immobilisation
progesterone receptor
platelet-rich plasma concentrate
Pierre Robin sequence
Predictive Salvage Index
posterior superior iliac spine
prothrombin time
pronator teres

xiii

xiv

Abbreviations

PTCH
PTEN
PTFE
RA
RA
RAPD
RCT
REE
RF
RFAL
RFF
RICH
RND
ROOF
RSTL
SAL
SAN
SCAP
SCC
SCIA
SCM
SEPS
SFS
SGAP
SHH
SIEA
SIRS
SJS
SLE
SLL
SLNB
SMAS
SNAP
SNAP
SND
SNUC
SOOF
SPAIR
SRY
SSD
SSM
SSSS
STIR
STL

patched (gene)
phosphatase and tensin homolog (gene)
polytetrafluoroethylene
rectus abdominis
rheumatoid arthritis
relative afferent pupillary defect
randomised controlled trial
resting energy expenditure
rheumatoid factor
radiofrequency assisted liposuction
radial forearm flap
rapidly involuting congenital haemangioma
radical neck dissection
retro-orbicularis oculi fat (pad)
relaxed skin tension line
suction-assisted liposuction
spinal accessory nerve
syringocystadenoma papilliferum
squamous cell carcinoma
superficial circumflex iliac artery
sternocleidomastoid
subfascial endoscopic perforating vein surgery
superficial fascial system
superior gluteal artery perforator (flap)
sonic hedgehog
superficial inferior epigastric artery (flap)
systemic inflammatory response syndrome
Stevens-Johnson syndrome
systemic lupus erythematosus
scapholunate ligament
sentinel lymph node biopsy
superficial muscular aponeurotic system
sensory nerve action potential
synaptosomal-associated protein
selective neck dissection
sinonasal undifferentiated carcinoma
suborbicularis oculi fat (pad)
short scar periareolar inferior pedicle reduction
sex-determining region of the Y chromosome
silver sulfadiazine
skin sparing mastectomy
staphylococcal scalded skin syndrome
short T1 inversion recovery
superior temporal line

Abbreviations

STS
STT
TA
TAM
TAR
TB
TBSA
TCA
TDA
TDAP
TED
TEN
TF
TFL
TGF
TIMP
TIP
TMJ
TNF
TNM
TNMG
TOS
t-PA
TPN
TRAM
TRT
TSS
TSST
TUG
TWIST
UAL
UCL
UK
USA
USP
UV
USS
VAIN
VASER
VCA
VEGF
VEGFR
VF
VIN

soft tissue sarcoma
scaphotrapezium-trapezoid
transversus abdominis
total active motion
thrombocytopenia – absent radius (syndrome)
tubercle bacillus
total body surface area
trichloroacetic acid
toluene diamine
thoracodorsal artery perforator
thromboembolic device
toxic epidermal necrolysis
tissue factor
tensor fasciae latae
transforming growth factor
tissue inhibitor of metalloproteinase
tubularised incised plate
temporomandibular joint
tumour necrosis factor
tumour, nodes, metastasis
tumour, nodes, metastasis, grade
thoracic outlet syndrome
tissue plasminogen activator
total parenteral nutrition
transverse rectus abdominis myocutaneous (flap)
thermal relaxation time
toxic shock syndrome
toxic shock syndrome toxin
transverse upper gracilis
twist family basic helix-loop-helix transcription factor (gene)
ultrasound-assisted liposuction
ulnar collateral ligament
United Kingdom
United States of America
United States Pharmacopeia
ultraviolet
ultrasound scan
vaginal intraepithelial neoplasia
Vibration Amplification of Sound Energy at Resonance
vascularised composite allotransplantation
vascular endothelial growth factor
vascular endothelial growth factor receptor
ventricular fibrillation
vulval intraepithelial neoplasia

xv

xvi

Abbreviations

VM
VMCM
VPI
VRAM
VRE
vWF
WHO
WLE
WNT7A
XP
YAG
ZF
ZM
ZPA

venous malformation
multiple cutaneous and mucosal venous malformations
velopharyngeal insufficiency
vertical rectus abdominis myocutaneous (flap)
vancomycin resistant Enterococcus
von Willebrand factor
World Health Organisation
wide local excision
wingless-type MMTV integration site family, member 7A
xeroderma pigmentosa
yttrium aluminium garnet
zygomaticofrontal
zygomaticomaxillary
zone of polarising activity

CHAPTER 1

General Principles
CHAPTER CONTENTS
Embryology, structure and function of the skin, 1
Blood supply to the skin, 5
Classification of flaps, 9
Geometry of local flaps, 13
Wound healing and skin grafts, 22
Bone healing and bone grafts, 31
Cartilage healing and cartilage grafts, 35
Nerve healing and nerve grafts, 36
Tendon healing, 41
Transplantation, 42
Tissue engineering, 47
Alloplastic implantation, 48
Wound dressings, 53
Sutures and suturing, 55
Tissue expansion, 57
Lasers, 61
Local anaesthesia, 65
Microsurgery, 69
Haemostasis and thrombosis, 74
Further reading, 77

Embryology, structure and function of the skin
• Skin differentiates from ectoderm and mesoderm during the 4th week.
• Skin gives rise to:
∘ Teeth and hair follicles, derived from epidermis and dermis
∘ Fingernails and toenails, derived from epidermis only.
• Hair follicles, sebaceous glands, sweat glands, apocrine glands and mammary glands are
‘epidermal appendages’ because they develop as ingrowths of epidermis into dermis.
• Functions of skin:
1 Physical protection
2 Protection against UV light
3 Protection against microbiological invasion
4 Prevention of fluid loss

Key Notes on Plastic Surgery, Second Edition. Adrian Richards and Hywel Dafydd.
© 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.

1

2

Chapter 1

5 Regulation of body temperature
6 Sensation
7 Immunological surveillance.

Epidermis

Papillary dermis
Reticular dermis
Subcutaneous tissue

Arrector pili muscle
Sebaceous gland
Hair bulb
Eccrine sweat gland

The epidermis
• Composed of stratified squamous epithelium.
• Derived from ectoderm.
• Epidermal cells undergo keratinisation – their cytoplasm is replaced with keratin as the
cell dies and becomes more superficial.
• Rete ridges are epidermal thickenings that extend downward between dermal papillae.
• Epidermis is composed of these five layers, from deep to superficial:
1 Stratum germinativum
∘ Also known as the basal layer.
∘ Cells within this layer have cytoplasmic projections (hemidesmosomes), which firmly
link them to the underlying basal lamina.
∘ The only actively proliferating layer of skin.
∘ Stratum germinativum also contains melanocytes.
2 Stratum spinosum
∘ Also known as the prickle cell layer.
∘ Contains large keratinocytes, which synthesise cytokeratin.
∘ Cytokeratin accumulates in aggregates called tonofibrils.
∘ Bundles of tonofibrils converge into numerous desmosomes (prickles), forming strong
intercellular contacts.
3 Stratum granulosum
∘ Contains mature keratinocytes, with cytoplasmic granules of keratohyalin.
∘ The predominant site of protein synthesis.
∘ Combination of cytokeratin tonofibrils with keratohyalin produces keratin.
4 Stratum lucidum
∘ A clear layer, only present in the thick glabrous skin of palms and feet.

General Principles

3

5 Stratum corneum
∘ Contains non-viable keratinised cells, having lost their nuclei and cytoplasm.
∘ Protects against trauma.
∘ Insulates against fluid loss.
∘ Protects against bacterial invasion and mechanical stress.

Cellular composition of the epidermis
• Keratinocytes – the predominant cell type in the epidermis.
• Langerhans cells – antigen-presenting cells (APCs) of the immune system.
• Merkel cells – mechanoreceptors of neural crest origin.
• Melanocytes – neural crest derivatives:
∘ Usually located in the stratum germinativum.
∘ Produce melanin packaged in melanosomes, which is delivered along dendrites to
surrounding keratinocytes.
∘ Melanosomes form a cap over the nucleus of keratinocytes, protecting DNA from
UV light.

The dermis
Accounts for 95% of the skin’s thickness.
Derived from mesoderm.
Papillary dermis is superficial; contains more cells and finer collagen fibres.
Reticular dermis is deeper; contains fewer cells and coarser collagen fibres.
It sustains and supports the epidermis.
Dermis is composed of:
Collagen fibres
∘ Produced by fibroblasts.
∘ Through cross-linking, are responsible for much of the skin’s strength.
∘ The normal ratio of type 1 to type 3 collagen is 5:1.
2 Elastin fibres
∘ Secreted by fibroblasts.
∘ Responsible for elastic recoil of skin.
3 Ground substance
∘ Consists of glycosaminoglycans (GAGs): hyaluronic acid, dermatan sulphate, chondroitin sulphate.
∘ GAGs are secreted by fibroblasts and become ground substance when hydrated.
4 Vascular plexus
∘ Separates the denser reticular dermis from the overlying papillary dermis.
•
•
•
•
•
•
1

Skin appendages
Hair follicles
• Each hair is composed of a medulla, a cortex and an outer cuticle.
• Hair follicles consist of an inner root sheath (derived from epidermis), and an outer root
sheath (derived from dermis).

4

Chapter 1

• Several sebaceous glands drain into each follicle.
∘ Drainage of the glands is aided by contraction of arrector pili muscles.
• Vellus hairs are fine and downy; terminal hairs are coarse.
• Hairs are either in anagen (growth), catagen (regressing), or telogen (resting) phase.
∘ <90% are in anagen, 1–2% in catagen and 10–14% in telogen at any one time.

Eccrine glands
• These sweat glands secrete odourless hypotonic fluid.
• Present in almost all sites of the body.
• Occur more frequently in the palm, sole and axilla.
Apocrine glands
• Located in axilla and groin.
• Emit a thicker secretion than eccrine glands.
• Responsible for body odour; do not function before puberty.
• Modified apocrine glands are found in the external ear (ceruminous glands) and eyelid
(Moll glands).
• The mammary gland is a modified apocrine gland specialised for manufacture of colostrum
and milk.
• Hidradenitis suppurativa is a disease of apocrine glands.
Sebaceous glands
• Holocrine glands that drain into the pilosebaceous unit in hair-bearing skin.
• They drain directly onto skin in the labia minora, penis and tarsus (meibomian glands).
• Most prevalent on forehead, nose and cheek; absent from palms and soles.
• Produce sebum, which contains fats and their breakdown products, wax esters and debris
of dead fat-producing cells.
∘ Sebum is bactericidal to staphylococci and streptococci.
• Sebaceous glands are not the sole cause of so-called sebaceous cysts.
• These cysts are in fact of epidermal origin and contain all substances secreted by skin
(predominantly keratin).
∘ Some maintain they should therefore be called epidermoid cysts.
Types of secretion from glands
• Eccrine or merocrine glands secrete opened vesicles via exocytosis.
• Apocrine glands secrete by ‘membrane budding’ – pinching off part of the cytoplasm in
vesicles bound by the cell’s own plasma membrane.
• Holocrine gland secretions are produced within the cell, followed by rupture of the cell’s
plasma membrane.

Histological terms
• Acanthosis: epidermal hyperplasia.
• Papillomatosis: increased depth of corrugations at the dermoepidermal junction.
• Hyperkeratosis: increased thickness of the keratin layer.

General Principles

5

• Parakeratosis: presence of nucleated cells at the skin surface.
• Pagetoid: when cells invade the upper epidermis from below.
• Palisading: when cells are oriented perpendicular to a surface.

Blood supply to the skin
• Epidermis contains no blood vessels.
• It is dependent on dermis for nutrients, supplied by diffusion.

Anatomy of the circulation
• Blood reaching the skin originates from named deep vessels.
• These feed interconnecting vessels, which supply the vascular plexuses of fascia, subcutaneous tissue and skin.

Deep vessels
• Arise from the aorta and divide to form the main arterial supply to head, neck, trunk
and limbs.
Interconnecting vessels
• The interconnecting system is composed of:
∘ Fasciocutaneous (or septocutaneous) vessels
– Reach the skin directly by traversing fascial septa.
– Provide the main arterial supply to skin in the limbs.
• Musculocutaneous vessels
∘ Reach the skin indirectly via muscular branches from the deep system.
∘ These branches enter muscle bellies and divide into multiple perforating branches,
which travel up to the skin.
∘ Provide the main arterial supply to skin of the torso.
Vascular plexuses of fascia, subcutaneous tissue and skin
1 Subfascial plexus
∘ Small plexus lying on the undersurface of deep fascia.
2 Prefascial plexus
∘ Larger plexus superficial to deep fascia; prominent on the limbs.
∘ Predominantly supplied by fasciocutaneous vessels.
3 Subcutaneous plexus
∘ At the level of superficial fascia.
∘ Mainly supplied by musculocutaneous vessels.
∘ Predominant on the torso.
4 Subdermal plexus
∘ Receives blood from the underlying plexuses.
∘ The main plexus supplying blood to skin.
∘ Accounts for dermal bleeding observed in incised skin.

6

Chapter 1

5 Dermal plexus
∘ Mainly composed of arterioles.
∘ Plays an important role in thermoregulation.
6 Subepidermal plexus
∘ Contains small vessels without muscle in their walls.
∘ Predominantly nutritive and thermoregulatory function.

Angiosomes
•
•
•
•
•
•
•
•

An angiosome is a three-dimensional composite block of tissue supplied by a named artery.
The area of skin supplied by an artery was first studied by Manchot in 1889.
His work was expanded by Salmon in the 1930s, and more recently by Taylor and Palmer.
The anatomical territory of an artery is the area into which the vessel ramifies before
anastomosing with adjacent vessels.
The dynamic territory of an artery is the area into which staining extends after intravascular infusion of fluorescein.
The potential territory of an artery is the area that can be included in a flap if it is delayed.
Vessels that pass between anatomical territories are called choke vessels.
The transverse rectus abdominis myocutaneous (TRAM) flap illustrates the angiosome
concept well:

Zone 1
• Receives musculocutaneous perforators from the deep inferior epigastric artery (DIEA)
and is therefore in its anatomical territory.
Zones 2 and 3
• There is controversy as to which of the following zones is 2 and which is 3.
• Hartrampf’s 1982 description has zone 2 across the midline and zone 3 lateral to zone 1.
∘ Holm’s 2006 study shows the opposite to be true.
• Skin lateral to zone 1 is in the anatomical territory of the superficial circumflex iliac artery
(SCIA).
∘ Blood has to travel through a set of choke vessels to reach it from the ipsilateral DIEA.
• Skin on the contralateral side of the linea alba is in the anatomical area of the ipsilateral
DIEA.
∘ It is also within the dynamic territory of the contralateral DIEA.
∘ This allows a TRAM flap to be reliably perfused based on either DIEA.
Zone 4
• This lies furthest from the pedicle and is in the anatomical territory of the contralateral
SCIA.
• Blood passing from the pedicle to zone 4 has to cross two sets of choke vessels.
• This portion of the TRAM flap has the worst blood supply and is often discarded.

Arterial characteristics
• Taylor made the following observations from his detailed anatomical dissections:
∘ Vessels usually travel with nerves.
∘ Vessels obey the law of equilibrium – if one is small, its neighbour will tend to be large.

General Principles

∘
∘
∘

7

Vessels travel from fixed to mobile tissue.
Vessels have a fixed destination but varied origin.
Vessel size and orientation is a product of growth.

Venous characteristics
• Venous networks consist of linked valvular and avalvular channels that allow equilibrium
of flow and pressure.
• Directional veins are valved; typically found in subcutaneous tissues of limbs or as a stellate
pattern of collecting veins.
• Oscillating avalvular veins allow free flow between valved channels of adjacent venous
territories.
∘ They mirror and accompany choke arteries.
∘ They define the perimeter of venous territories in the same way choke arteries define
arterial territories.
• Superficial veins follow nerves; perforating veins follow perforating arteries.

The microcirculation
• Terminal arterioles are found in reticular dermis.
∘ They terminate as they enter the capillary network.
• The precapillary sphincter is the last part of the arterial tree containing muscle within its
wall.
∘ It is under neural control and regulates blood flow into the capillary network.
• The skin’s blood supply far exceeds its nutritive requirements.
• It bypasses capillary beds via arteriovenous anastomoses (AVAs) and has a primarily thermoregulatory function.
∘ AVAs connect arterioles to efferent veins.
• AVAs are of two types:
1 Indirect AVAs – convoluted structures known as glomera (sing. glomus)
– Densely innervated by autonomic nerves.
2 Direct AVAs – less convoluted with sparser autonomic supply.

Control of blood flow
• The muscular tone of vessels is controlled by:

Pressure of the blood within vessels (myogenic theory)
• Originally described by Bayliss, states that:
∘ Increased intraluminal pressure results in constriction of vessels.
∘ Decreased intraluminal pressure results in their dilatation.
• Helps keep blood flow constant; accounts for hyperaemia on release of a tourniquet.
Neural innervation
• Arterioles, AVAs and precapillary sphincters are sympathetically innervated.
• Increased arteriolar tone results in decreased cutaneous blood flow.
• Increased precapillary sphincter tone reduces blood flow into capillary networks.
• Decreased AVA tone increases non-nutritive blood flow bypassing the capillary bed.

8

Chapter 1

Humoral factors
• Epinephrine, norepinephrine, serotonin, thromboxane A2 and prostaglandin F2α cause
vasoconstriction.
• Histamine, bradykinin and prostaglandin E1 cause vasodilatation.
• Low O2 saturation, high CO2 saturation and acidosis also cause vasodilatation.
Temperature
• Heat causes cutaneous vasodilatation and increased flow, which predominantly bypasses
capillary beds via AVAs.

The delay phenomenon
• Delay is any preoperative manoeuvre that results in increased flap survival.
• Historical examples include Tagliacozzi’s nasal reconstruction described in the 16th
century.
∘ Involves elevation of a bipedicled flap with length : breadth ratio of 2:1.
∘ The flap can be considered as two 1:1 flaps.
∘ Cotton lint is placed under the flap, preventing its reattachment.
∘ Two weeks later, one end of the flap is detached from the arm and attached to the nose.
– A flap of these dimensions transferred without a delay procedure would have a significant chance of distal necrosis.
• Delay is occasionally used for pedicled TRAM breast reconstruction.
∘ The DIEA is ligated two weeks prior to flap transfer.
• The mechanism of delay remains incompletely understood.
• These theories have been proposed to explain the delay phenomenon:

Increased axiality of blood flow
• Removal of blood flow from the periphery of a random flap promotes development of an
axial blood supply from its base.
• Axial flaps have improved survival compared to random flaps.
Tolerance to ischaemia
• Cells become accustomed to hypoxia after the initial delay procedure.
• Less tissue necrosis therefore occurs after the second operation.
Sympathectomy vasodilatation theory
• Dividing sympathetic fibres at the borders of a flap results in vasodilatation and improved
blood supply.
• But why, if sympathectomy is immediate, does the delay phenomenon only begin to
appear at 48 hours, and why does it take 2 weeks for maximum effect?
Intraflap shunting hypothesis
• Postulates that sympathectomy dilates AVAs, resulting in an increase in nonnutritive blood
flow bypassing the capillary bed.
• A greater length of flap will survive at the second stage as there are fewer sympathetic
fibres to cut and therefore less of a reduction in nutritive blood flow.

General Principles

9

Hyperadrenergic state
• Surgery results in increased tissue concentrations of vasoconstrictors, such as epinephrine
and norepinephrine.
• After the initial delay procedure, the resultant reduction in blood supply is not sufficient
to produce tissue necrosis.
∘ The level of vasoconstrictor substances returns to normal before the second procedure.
• The second procedure produces another rise in the concentration of vasoconstrictor substances.
∘ This rise is said to be smaller than it would be if the flap were elevated without a prior
delay.
• The flap is therefore less likely to undergo distal necrosis after a delay procedure.
Unifying theory
• Described by Pearl in 1981; incorporates elements of all these theories.

Classification of flaps
• Flaps can be classified by the five ‘C’s:
∘ Circulation
∘ Composition
∘ Contiguity
∘ Contour
∘ Conditioning.

Circulation
• Can be further subcategorised into:
∘ Random
∘ Axial (direct, fasciocutaneous, musculocutaneous, or venous).

Random flaps
• No directional blood supply; not based on a named vessel.
• These include most local flaps on the face.
• Should have a maximum length : breadth ratio of 1:1 in the lower extremity, as it has a
relatively poor blood supply.
∘ Can be up to 6:1 in the face, as it has a good blood supply.
Axial flaps
Direct
• Contain a named artery running in subcutaneous tissue along the axis of the flap.
• Examples include:
∘ Groin flap, based on superficial circumflex iliac vessels.
∘ Deltopectoral flap, based on perforating vessels of internal mammary artery.
• Both flaps can include a random segment in their distal portions after the artery peters
out.

10

Chapter 1

Fasciocutaneous
• Based on vessels running either within or near the fascia.
• The fasciocutaneous system predominates on the limbs.
• Fasciocutaneous flaps are classified by Cormack and Lamberty:
Type A
• Dependent on multiple non-named fasciocutaneous vessels that enter the base of the flap.
• Lower leg ‘super flaps’ described by Pontén are examples of type A flaps.
∘ Their dimensions vastly exceed the 1:1 ratios recommended.
Type B
• Based on a single fasciocutaneous vessel, which runs along the axis of the flap.
• Examples include scapular/parascapular flap, and perforator-based fasciocutaneous flaps
of the lower leg.
Type C
• Supplied by multiple small perforating vessels, which reach the flap from a deep artery
running along a fascial septum between muscles.
• Examples include radial forearm flap (RFF) and lateral arm flap.
Type C flaps with bone
• Osteofasciocutaneous flaps, originally classified as type D.
• Examples include:
∘ RFF raised with a segment of radius; lateral arm flap raised with a segment of humerus.
• The Mathes and Nahai fasciocutaneous flap classification is slightly different:
Type A
• Direct cutaneous pedicle.
• Examples: groin, superficial inferior epigastric and dorsal metacarpal artery flaps.
Type B
• Septocutaneous pedicle.
• Examples: scapular and parascapular, lateral arm, posterior interosseous flap.
Type C
• Musculocutaneous pedicle.
• Examples: median forehead, nasolabial and (usually) anterolateral thigh flap.
Musculocutaneous
• Flaps based on perforators that reach the skin through the muscle.
• The musculocutaneous system predominates on the torso.
• Muscle and musculocutaneous flaps were classified by Mathes and Nahai in 1981:

General Principles

11

Type I
• Single vascular pedicle.
• Examples: gastrocnemius, tensor fasciae latae (TFL), abductor digiti minimi.
• Good flaps for transfer – the whole muscle is supplied by a single pedicle.
Type II
• Dominant pedicle(s) and other minor pedicle(s).
• Examples: trapezius, soleus, gracilis.
• Good flaps for transfer – can be based on the dominant pedicle after the minor pedicle(s)
are ligated.
• Circulation via minor pedicles alone is not reliable.
Type III
• Two dominant pedicles, each arising from a separate regional artery or opposite sides of
the muscle.
• Examples: rectus abdominis, pectoralis minor, gluteus maximus.
• Useful muscles for transfer – can be based on either pedicle.
Type IV
• Multiple segmental pedicles.
• Examples: sartorius, tibialis anterior, long flexors and extensors of the toes.
• Seldom used for transfer – each pedicle supplies only a small portion of muscle.
Type V
• One dominant pedicle and secondary segmental pedicles.
• Examples: latissimus dorsi, pectoralis major.
• Useful flaps – can be based on either the dominant pedicle or secondary segmental
pedicles.
Venous
• Based on venous, rather than arterial, pedicles.
• In fact, many venous pedicles have small arteries running alongside them.
• The mechanism of perfusion is not completely understood.
• Example: saphenous flap, based on long saphenous vein.
∘ Used to reconstruct defects around the knee.
• Venous flaps are classified by Thatte and Thatte:
Type 1
• Single venous pedicle.
Type 2
• Venous flow-through flaps, supplied by a vein that enters one side of the flap and exits
from the other.

12

Chapter 1

Type 3
• Arterialised through a proximal arteriovenous anastomosis and drained by distal veins.
• Venous flaps tend to become congested post-operatively.
• Survival is inconsistent; they have therefore not been universally accepted.
• Modifying the type 3 arterialised venous flap by restricting direct arteriovenous shunting
can improve survival rates by redistributing blood to the periphery of the flap.

Composition
• Flaps can be classified by their composition as:
∘ Cutaneous
∘ Fasciocutaneous
∘ Fascial
∘ Musculocutaneous
∘ Muscle only
∘ Osseocutaneous
∘ Osseous.

Contiguity
• Flaps can be classified as:
∘ Local flaps
– Composed of tissue adjacent to the defect.
∘ Regional flaps
– Composed of tissue from the same region of the body as the defect, e.g. head and
neck, upper limb.
∘ Distant flaps
– Pedicled distant flaps come from a distant part of the body to which they remain
attached.
– Free flaps are completely detached from the body and anastomosed to recipient
vessels close to the defect.

Contour
• Flaps can be classified by the way they are transferred into the defect:

Advancement
• Stretching the flap
• Excision of Burow triangles at the flap’s base
• V-Y advancement
• Z-plasty at its base
• Careful scoring of the undersurface
• Combinations of the above.
Transposition
• The flap is moved into an adjacent defect, leaving a secondary defect that must be closed
by another method.

General Principles

13

Rotation
• The flap is rotated into the defect.
• Classically, rotation flaps are designed to allow closure of the donor defect.
• In reality, many flaps have elements of transposition and rotation, and may be best
described as pivot flaps.
Interpolation
• The flap is moved into a defect either under or above an intervening bridge of tissue.
Crane principle
• This aims to transform an ungraftable bed into one that will accept a skin graft.
• At the first stage, a flap is placed into the defect.
• After sufficient time to allow vascular ingrowth into the flap from the recipient site, a
superficial part of the flap is replaced in its original position.
• This leaves a segment of subcutaneous tissue in the defect, which can now accept a skin
graft.

Conditioning
• This involves delaying the flap, discussed in ‘Blood supply to the skin’.

Geometry of local flaps
Orientation of elective incisions
• In the 19th century, Langer showed that circular awl wounds produced elliptical defects
in cadaver skin.
• He believed this occurred because skin tension along the longitudinal axis of the ellipse
exceeded that along the transverse axis.
• Borges has provided over 36 descriptive terms for skin lines, including:
∘ Relaxed skin tension lines (RSTLs) – these are parallel to natural skin wrinkles (rhytids)
and tend to be perpendicular to the fibres of underlying muscles.
∘ Lines of maximum extensibility (LME) – these lie perpendicular to RSTLs and parallel
to the fibres of underlying muscles.
• The best orientation of an incision can be judged by a number of methods:
∘ Knowledge of the direction of pull of underlying muscles.
∘ Making the incision parallel to any rhytids or RSTLs.
∘ Making the incision perpendicular to LMEs.
∘ Making the incision parallel to the direction of hair growth.
∘ ‘The pinch test’ – if skin either side of the planned incision is pinched, it forms a transverse fold without distortion if it is orientated correctly; if a sigmoid-shaped fold forms,
it is orientated incorrectly.

Plasty techniques
Z-plasty
• Involves transposition of two adjacent triangular-shaped flaps.

14

Chapter 1

• Can be used to:
∘ Increase the length of an area of tissue or scar
∘ Break up a straight-line scar
∘ Realign a scar.
• The degree of elongation of the longitudinal axis of the Z-plasty is directly related to the
angles of its constituent flaps.
∘ 30∘ → 25% elongation
∘ 45∘ → 50% elongation
∘ 60∘ → 75% elongation
∘ 75∘ → 100% elongation
∘ 90∘ → 125% elongation.
• The amount of elongation can be worked out by starting at 30∘ and 25% and adding 15∘
and 25% to each of the figures.
• Gains in length are estimates; true values depend on local tissue elasticity and tension.
• Flaps with 60∘ angles are most commonly used as they lengthen without undue tension.
• The angles of the two flaps need not be equal and can be designed to suit local tissue
requirements.
∘ However, all three limbs should be of the same length.
• When designing a Z-plasty to realign a scar:
1 Mark the desired direction of the new scar.
2 Draw the central limb of the Z-plasty along the original scar.
3 Draw the lateral limbs of the Z-plasty from the ends of the central limb, to the line
drawn in (1).
4 Two patterns will be available, one with a wide angle at the apex of the flaps, the other
with a narrow angle.
5 Select the pattern with the narrower angle as these flaps transpose better.

General Principles

15

The four-flap plasty
• It is, in effect, two interdependent Z-plasties.
• Can be designed with different angles.
• The two outer flaps become the inner flaps after transposition.
• The two inner flaps become the outer flaps after transposition.
• The flaps, originally in an ‘ABCD’ configuration, end as ‘CADB’ (CADBury).

C

A

A

B

A
C

or

A

B
C

D

D

C

D

D

B
B

The five-flap plasty
• Because of its appearance, this is also called a jumping-man flap.
• Used to release first web space contractures and epicanthal folds.
• It is, in effect, two opposing Z-plasties with a V-Y advancement in the center.
• The flaps, originally in an ‘ABCDE’ configuration, end as ‘BACED’.

A

E
B

C

D

B

C
A

D
E

The W-plasty
• Used to break up the line of a scar and improve its aesthetics.
• Unlike the Z-plasty, it does not lengthen tissue.
• If possible, one of the limbs of the W-plasty should lie parallel to the RSTLs so that half of
the resultant scar will lie parallel to them.
• Using a template helps ensure each wound edge interdigitates easily.
• The technique discards normal tissue, which may be a disadvantage in certain areas.

16

Chapter 1

RSTL

Local flaps
• Advancement flaps (simple, modified, V-Y, keystone, bipedicled).
• Pivot flaps (transposition, interpolation, rotation, bilobed).

Advancement flaps
Simple
• Rely on skin elasticity.

General Principles

Modified
• Incorporate one of the following at the flap’s base to increase advancement:
∘ Counter incision
∘ Excision of Burow’s triangle
∘ Z-plasty.
Counter incision
at base

Burow's triangle
at base

Z-plasty
at base

V-Y
• These are incised along their cutaneous borders.
• Their blood supply comes from deep tissue through a subcutaneous pedicle.
• Horn flaps and oblique V-Y flaps are modifications of the original V-Y.

17

18

Chapter 1

Traditional V-Y flap

Horn flap

Keystone
• Trapezoidal flaps used to close elliptical defects.
• Essentially two V-Y flaps end-to-side.
• Designed to straddle longitudinal structures, e.g. superficial nerves and veins, which are
incorporated into the flap.
• Blunt dissection to deep fascia preserves perforators and subcutaneous veins.
• The lateral deep fascial margin can be incised for increased mobilisation.
• The extremes of the donor site are closed as V-Y advancements, which produces transverse
laxity in the flap.

General Principles

V-Y
closure

90°
x

x
V-Y
closure

90°

Bipedicled
• Receive blood supply from both ends.
• Less prone to necrosis than flaps of similar dimensions attached only at one end.
• Example: von Langenbeck mucoperiosteal flap, used to repair cleft palates.
• Bipedicled flaps are designed to curve parallel with the defect.
∘ This permits flap transposition with less tension.

Original
defect
2x

x
y

2y
2x

Secondary
defect

19

20

Chapter 1

Pivot flaps
Transposition flaps
• Transposed into the defect, leaving a donor site that is closed by some other means (often
a skin graft).

Line of
greatest
tension
Area of
excess
skin or
dog ear

Pivot
point

Secondary
defect

Transposition flaps with direct closure of donor site
• Include the rhomboid flap (Limberg flap) and Dufourmentel flap.
• These are similar in concept but vary in geometry.
• Both are designed to leave the donor site scar parallel to RSTLs.
The rhomboid flap

The rhomboid flap
Excised area
x

x

120°

60°

Lo x
o
ski se
n
RS

TL

LM
E

x

x
60°

x

General Principles

The Dufourmentel flap

The Dufourmentel flap
Long
diagonal

y

b
a
c

x°

y

Extended side
of defect

b
x°

y

a

Short diagonal

c

Parallel to long
diagonal

Interpolation flaps
• Flaps raised from local, but not adjacent, skin.
• The pedicle is passed either over or under an intervening skin bridge.

Defect

Intact skin bridge

Skin
paddle

De-epithelialised
skin pedicle
Pivot point

Rotation flaps
• These large flaps rotate tissue into the defect.
• Tissue redistribution usually permits direct closure of the donor site.
• Flap circumference should be 5–8 times the width of the defect.
• These are used on the scalp for hair-bearing reconstruction.
• The back cut at the flap’s base can be directed towards or away from the defect.

21

22

Chapter 1

Back cut

Burow's triangle
x
x

2x
Pivot point

The bilobed flap
• Various designs have been described.
• Consists of two transposition flaps.
• The first flap is transposed into the original defect.
• The second flap is transposed into the secondary defect – the donor site of the first flap.
• The tertiary defect at the donor site of the second flap closes directly.
∘ This suture line is designed to lie parallel to RSTLs.
• Esser, who first described the flap, put the first flap at 90∘ to the defect and the second
flap at 90∘ to the first flap.
• Zitelli modified these angles to 45∘ each, resulting in smaller dog ears.
(a)

Defect

r
r

Pivot point
(b)

(c)

RSTL

Wound healing and skin grafts
• Healing by primary intention
∘ Skin edges are directly opposed.
∘ Healing is normally good, with minimal scar formation.

General Principles

23

• Healing by secondary intention
∘ The wound is left open to heal by a combination of granulation tissue formation, contraction and epithelialisation.
∘ More inflammation and proliferation occurs compared to primary healing.
• Healing by tertiary intention
∘ Wounds are initially left open, then closed as a secondary procedure.

Phases of wound healing
1
2
3
4

Haemostasis
Inflammation
Proliferation
Remodelling.

Haemostasis
• Vasoconstriction occurs immediately after vessel division due to release of thromboxanes
and prostaglandins from damaged cells.
• Platelets bind to exposed collagen, forming a platelet plug.
• Platelet degranulation activates more platelets and increases their affinity to bind
fibrinogen.
∘ Involves modification of membrane glycoprotein IIb/IIIa (blocked by clopidogrel).
• Platelet activating factor (PAF), von Willebrand factor (vWF) and thromboxane A2 stimulate conversion of fibrinogen to fibrin.
∘ This propagates formation of thrombus.
• Thrombus is initially pale when it contains platelets alone (white thrombus).
• As red blood cells are trapped, the thrombus becomes darker (red thrombus).
Inflammation
• Occurs in the first 2–3 days after injury.
• Stimulated by physical injury, antigen–antibody reaction or infection.
• Platelets release growth factors, e.g. platelet-derived growth factor (PDGF).
∘ Also release proinflammatory factors, e.g. serotonin, bradykinin, prostaglandins, thromboxanes and histamine.
∘ These increase cell proliferation and migration.
• Endothelial cells swell, causing vasodilatation and allowing egress of polymorphonuclear
neutrophils (PMNs) and monocytes into the tissue.
• T lymphocytes migrate into the wound under the influence of interleukin-1.
• Lymphocytes secrete various cytokines, including epidermal growth factor and basic
fibroblast growth factor (bFGF).
∘ They also play a role in cellular immunity and antibody production.
Proliferation
• Begins on the 2nd or 3rd day and lasts for 2–4 weeks.
• Monocytes mature into macrophages that release PDGF and transforming growth factor-β
(TGF-β), which are chemoattractant to fibroblasts.
• Fibroblasts, usually located in perivascular tissue, migrate along fibrin networks into the
wound.

24

Chapter 1

• Fibroblasts secrete GAGs to produce ground substance, and then produce collagen and
elastin.
∘ Initially, type III collagen is produced to increase the strength of the wound.
• Some fibroblasts differentiate into myofibroblasts and effect wound contraction.
• Angiogenesis occurs concurrently to supply oxygen and nutrients to the wound.
∘ Endothelial stem cells from blood vessels migrate through extracellular matrix.
∘ Attracted to the wound by angiogenic factors, thrombus and local hypoxia.
• Zinc-dependent matrix metalloproteinases aid cell migration through tissues.

Remodelling
• Begins 2–4 weeks after injury and can last a year or longer.
• During remodelling there is no net increase in collagen (collagen homeostasis).
• Type III collagen is replaced by the stronger type I collagen.
• Collagen fibres, initially laid down haphazardly, are arranged in a more organised
manner.
• The wound’s tensile strength approaches 50% of normal by 3 months; eventually becomes
80% as strong.
• The extensive capillary network is no longer required and is removed by apoptosis, leaving
a pale collagen scar.

Abnormal scars
• Classified as either hypertrophic or keloid.
∘ Keloids extend beyond the original wound margins.
∘ Hypertrophic scars are limited to original wound margins; commoner than keloids.
• Increased numbers of mast cells in abnormal scars may account for the pruritus experienced by some patients.

Hypertrophic scars
• Usually occurs within 8 weeks of wounding.
• Grow rapidly for up to 6 months before gradually regressing to a flat, asymptomatic scar.
∘ This may take a few years.
• Typically form at locations under tension, e.g. shoulders, neck, presternal area, knees,
ankles.
• Microscopy shows well-organised type III collagen bundles with nodules containing
myofibroblasts.
Keloid scars
• Dark-skinned individuals are more prone to keloid scars.
• There is often a family history.
• May develop at any point up to several years after minor injuries.
• Typically persist for long periods of time and do not regress spontaneously.
• Pain and hypersensitivity are associated more with keloids than hypertrophic scars.
• Commonly form on anterior chest, shoulders, earlobes, upper arms and cheeks.
• Excision typically results in recurrence.

General Principles

25

• Microscopy shows poorly organised type I and III collagen bundles with few myofibroblasts.
• Expression of proliferating cell nuclear antigen (PCNA) and p53 is upregulated.

Epithelial repair
• If the epidermal basement membrane is not breached, epithelial cells are replaced by
upward migration of keratinocytes as in uninjured skin.
• If the basement membrane is breached, re-epithelialisation must occur from the wound
margins and, if present and intact, from epidermal appendages.
• Re-establishing epithelial continuity consists of these four phases:

Mobilisation
• Epithelial cells at the wound edges elongate, flatten and form pseudopodia.
• They detach from neighbouring cells and basement membrane.
Migration
• Decreased contact inhibition promotes cell migration.
• Epithelial cells climb over one another to migrate.
• As cells migrate, epithelial cells at the wound edge proliferate to replace them.
• Cells migrate until they meet those from the opposite wound edge.
• At this point, contact inhibition is reinstituted and migration ceases.
Mitosis
• Epithelial cells proliferate once they have covered the wound.
• They secrete proteins to form a new basement membrane.
• Cells reverse the morphological changes required for migration.
• Desmosomes and hemidesmosomes are re-established to anchor themselves to the basement membrane and to each other.
• This new epithelial cell layer forms a stratum germinativum and undergoes mitosis as in
normal skin.
Cellular differentiation
• The normal structure of stratified squamous epithelium is re-established.

Collagen
• Constitutes approximately 30% of total body protein.
• Formed by hydroxylation of amino acids lysine and proline by enzymes that require vitamin C as a cofactor.
• Procollagen is initially formed within the cell.
• Procollagen is transformed into tropocollagen after it is excreted from the cell.
• Fully formed collagen has a complex structure.
∘ Consists of three polypeptide chains wound in a left-handed helix.
∘ These three chains are further wound in a right-handed coil to form the basic tropocollagen unit.

26

Chapter 1

• Collagen formation is inhibited by colchicine, penicillamine, steroids and deficiencies of
vitamin C and iron.
• Cortisol stimulates degradation of skin collagen.
• Thus far, 28 types of collagen have been identified.
• Each type shares the same basic structure but differs in the relative composition of hydroxylysine and hydroxyproline, and in the degree of cross-linking between chains.
• The five most common types are:
∘ Type I: predominant in mature skin, bone and tendon.
∘ Type II: present in hyaline cartilage and cornea.
∘ Type III: present in healing tissue, particularly fetal wounds.
∘ Type IV: predominant constituent of basement membranes.
∘ Type V: similar to type IV. Also found in hair and placenta.
• The ratio of type I collagen to type III collagen in normal skin is 5:1.
∘ Hypertrophic and immature scars contain ratios of 2:1 or less.
• 90% of total body collagen is type I.

The macrophage
• Derived from mononuclear leukocytes.
• Debrides tissue and removes micro-organisms.
• Co-ordinates angiogenesis and fibroblast activity by releasing growth factors:
∘ PDGF, FGF 1 and 2, tumour necrosis factor alpha (TNF-α) and TGF-β.
• Essential for normal wound healing.
• Wounds depleted of macrophages heal slowly.

The myofibroblast
• First identified by Gabbiani in 1971.
• Differs from a fibroblast – contains cytoplasmic filaments of α-smooth muscle actin, which
are also found in smooth muscle.
• Actin fibres within myofibroblasts are thought to be responsible for wound contraction.
• The number of myofibroblasts within a wound is proportional to its contraction.
• Increased numbers have been found in the fascia of Dupuytren’s disease.
∘ Thought to be responsible for the abnormal contraction of this tissue.

TGF-𝛃
• Macrophages, fibroblasts, platelets, keratinocytes and endothelial cells secrete this growth
factor.
• Believed to play a central role in wound healing:
∘ Chemoattraction of fibroblasts and macrophages
∘ Induction of angiogenesis
∘ Stimulation of extracellular matrix deposition
∘ Keratinocyte proliferation.
• Three isoforms have been identified:
∘ Types 1 and 2 promote wound healing and scarring; upregulated in keloids.
∘ Type 3 decreases wound healing and scarring – may have a role as an antiscarring agent.

General Principles

27

• Fetal wounds have higher levels of TGF-β3 than adult wounds.
∘ TGF-β3 is thought to antagonise TGF-β1 and 2.
∘ May be one factor responsible for decreased inflammation and improved scarring
observed in fetal tissue.

Factors affecting healing
• Systemic
∘ Congenital
∘ Acquired
• Local.

Systemic factors: congenital
Pseudoxanthoma elasticum
• Autosomal recessive.
• Characterised by increased collagen degradation and mineralisation.
• Skin is pebbled and extremely lax.
• Most have premature arteriosclerosis in their 30s.
Ehlers–Danlos syndrome
• Heterogeneous collection of connective tissue disorders.
• Most are autosomal dominant.
• Results from defects in synthesis, structure or cross-linking of collagen.
• Clinical features:
∘ Hypermobile fingers
∘ Hyperextensible skin
∘ Fragile connective tissues.
• Surgery is avoided if possible – wound healing is poor.
Cutis laxa
• Presents in the neonatal period.
• Skin is abnormally lax.
• Patients have inelastic, coarsely textured, drooping skin.
Progeria
• Characterised by premature ageing.
• Clinical features:
∘ Growth retardation
∘ Wrinkled skin
∘ Baldness
∘ Atherosclerosis.
Werner syndrome
• Autosomal recessive.
• Skin changes similar to scleroderma.
• Elective surgery avoided whenever possible – healing is poor.

28

Chapter 1

Epidermolysis bullosa
• Heterogeneous collection of separate conditions.
• Skin is very susceptible to mechanical stress.
• Blistering may occur after minor trauma (Nikolsky sign).
• The most severe subtype, dermolytic bullous dermatosis (DBD), results in hand fibrosis
and syndactyly – the ‘mitten hand’ deformity.
• Patients may develop squamous cell carcinoma in areas of chronic erosion.

Systemic factors: acquired
Nutrition
• Vitamin A involved in collagen cross-linking; deficiency delays wound healing.
• Vitamin C required for collagen synthesis.
• Vitamin E acts as a membrane stabiliser; deficiency may inhibit healing.
• Zinc, copper and selenium are important cofactors for many enzymes; administration
accelerates healing in deficient states.
• Hypoalbuminaemia is associated with poor healing.
Pharmacological
• Steroids decrease inflammation and subsequent wound healing.
• Cytotoxics damage basal keratinocytes.
• Non-steroidal anti-inflammatory drugs (NSAIDs) decrease collagen synthesis.
• Anti-TNF-α drugs used in rheumatoid may increase post-operative wound complications.
Endocrine abnormalities
• Diabetics often have delayed wound healing; this is multifactorial.
• Untreated hypothyroidism is associated with slow healing.
Age
• Cell multiplication rates decrease with age.
∘ All stages of healing are therefore protracted.
• Healed wounds have decreased tensile strength in the elderly.
Smoking
• Nicotine is a sympathomimetic that causes vasoconstriction and consequently decreases
tissue perfusion.
• Carbon monoxide in cigarette smoke decreases oxygen-carrying capacity of haemoglobin.
• Hydrogen cyanide in cigarette smoke poisons intracellular oxidative metabolism
pathways.

Local factors
Infection
• Subclinical wound infection can impair wound healing.
• Wounds with >105 organisms per gram of tissue are considered infected and are unlikely
to heal without further treatment.

General Principles

29

Radiation
• Causes endothelial cell, capillary and arteriole damage.
• Irradiated fibroblasts secrete less collagen and extracellular matrix.
• Lymphatics are also damaged, resulting in oedema and an increased infection risk.
Blood supply
• Decreased tissue perfusion results in decreased wound oxygenation.
• Fibroblasts are oxygen-sensitive and their function is reduced in hypoxic tissue.
• Reduced oxygen delivery results from decreases in:
∘ Inspired oxygen concentration
∘ Oxygen transfer to haemoglobin
∘ Haemoglobin concentration
∘ Tissue perfusion.
• Decreased oxygen delivery to tissue reduces:
∘ Collagen formation
∘ Extracellular matrix deposition
∘ Angiogenesis
∘ Epithelialisation.
• Hyperbaric oxygen increases inspired oxygen concentration but its effectiveness relies on
good tissue perfusion.
Trauma
• The delicate neoepidermis of healing wounds is disrupted by trauma.
Neural supply
• There is evidence that wounds in denervated tissue heal slowly.
• May contribute to delayed healing observed in some pressure sores, and in patients with
diabetes and leprosy.
• Mechanisms are poorly understood, but may be related to levels of chemoattractant neuropeptides in the wound.

Fetal wound healing
• Tissue healing in the first 6 months of fetal life occurs by regeneration rather than scarring.
∘ Regenerative healing is characterised by absence of scarring.
• Normal dermal structures such as hair follicles form normally.
• Regenerative healing differs from adult healing:
∘ Reduced inflammation.
∘ Reduced platelet aggregation and degranulation.
∘ Reduced angiogenesis.
∘ Epithelialisation is more rapid.
∘ Virtually no myofibroblasts and no wound contraction.
∘ Collagen deposition is rapid, organised and not excessive.
∘ More type III than type I collagen is laid down.
∘ The wound contains more water and hyaluronic acid.
• Relative proportions of TGF-β isoforms may be responsible for some of these differences.

30

Chapter 1

Skin grafts
• Skin grafts are either full or split thickness.
• Split-skin grafts contain the epidermis and a variable amount of dermis.
∘ Usually harvested from thigh or buttock.
• Full-thickness skin grafts contain the entire epidermis and dermis.
∘ Usually harvested from areas that allow direct closure of the donor defect.
• Primary contraction is the immediate recoil observed in freshly harvested skin.
∘ Due to elastin in the dermis.
• Secondary contracture occurs after the graft has healed.
∘ Due to myofibroblast activity.
• The thicker the graft, the greater the degree of primary contraction.
• The thinner the graft, the greater the degree of secondary contracture.

Mechanisms
• Skin grafts heal in four phases:
Adherence
• Fibrin bonds form immediately on applying skin graft to a suitable bed.
Serum imbibition
• Grafts swell in the first 2–4 days after application.
• This results from absorption of fluid (serum imbibition).
• The nutritive value of serum imbibition in maintaining graft viability is debated.
Revascularisation
• After 48–72 hours, capillary buds from the recipient bed have formed a fine vascular
network in the fibrin layer between graft and wound.
• Vessel ingrowth into skin grafts begins around the 4th day.
• The mechanism of revascularisation is uncertain and may be via:
∘ Inosculation – direct anastomosis between vessels in the graft and those in recipient
tissue.
∘ Revascularisation – new vessel ingrowth from recipient tissue along the graft’s vascular
channels.
∘ Neovascularisation – new vessel ingrowth from recipient tissue along new channels in
the graft.
Remodelling
• The histological architecture of the graft returns to that of normal skin.

Reasons for graft failure
Haematoma
• Most common cause of graft failure.

General Principles

31

• Risk of haematoma formation is minimised by:
∘ Meticulous haemostasis
∘ Use of meshed skin graft, which allows blood to escape
∘ Application of a firm dressing.
Infection
• Generally, skin grafts will not take if the bacterial count of the recipient site exceeds 105
organisms per gram.
• Group A β-haemolytic Streptococcus can destroy grafts when present in much fewer
numbers.
∘ This ability is attributed to secretion of proteases, such as streptokinase and
hyaluronidase, which prevent adhesion.
Seroma
• Fluid collection under the graft reduces the likelihood of successful take.
Shear
• Lateral force applied to a graft.
• Results in disruption of the delicate connections between graft and bed.
Inappropriate bed
• Skin grafts will not survive on bare cartilage, tendon and endochondral bone denuded of
periosteum.
• Membranous bone, found in some areas of the skull, will accept a skin graft.
• Grafts on previously irradiated wound beds are prone to failure.
Technical error
• An assortment of technical errors can result in graft failure.
• Examples: upside down graft placement, graft desiccation.

Bone healing and bone grafts
• Bones are derived from mesenchyme.
• Composed of organic matrix (osteoid), which is mineralised by hydroxyapatite (a calcium
salt).
• Embryologically, bones form by one of two mechanisms.
1 Intramembranous ossification
∘ Occurs by deposition of bone within a vascularised membranous template.
∘ Examples: flat bones of the face, calvarium and ribs.
2 Endochondral ossification
∘ Develops from a cartilage precursor, or anlage.
– In German, Anlage means primordium, plan or template.
∘ Examples: all long bones and the iliac crest.

32

Chapter 1

Bone structure
• All bones have an outer cortical layer and an inner cancellous layer.
∘ The cancellous part of membranous bone is in the diploic space.
• Cancellous bone consists of loosely woven trabeculae of organic and inorganic bone.
• Cortical bone consists of:
∘ Multiple columnar bone units (osteons), composed of a central longitudinal canal
(Haversian canal) that contains a central blood vessel.
∘ Transverse nutrient canals (Volkmann canals) connecting adjacent osteons.
• Bone is laid down in concentric layers around each Haversian canal.
• Osteocytes are scattered throughout osteons, each within its own space (lacuna).

Blood supply to bone
1
2
3
4

Periosteal vessels at the sites of muscle attachment.
Apophyseal vessels at the sites of tendon and ligament attachment.
Nutrient arteries supplying the medullary cavity (endosteal supply).
Epiphyseal vessels supplying growth plates.

Bone healing
• The phases of bone healing are similar to those of wound healing.
1 Haematoma formation
2 Inflammation
– Fracture haematoma is gradually replaced by granulation tissue.
– Osteoclasts remove necrotic bone.
3 Cellular proliferation
– Stem cell recruitment.
– Periosteal proliferation occurs on the outer aspect of the cortex.
– Endosteal proliferation occurs on the inner aspect of the cortex.
4 Callus formation
– Callus consists of immature woven bone produced by osteoblasts and hyaline cartilage produced by chondroblasts.
– This soft callus (osteoid) is mineralised with hydroxyapatite to form hard callus
(mature woven bone).
5 Remodelling
– Woven bone is slowly replaced by lamellar bone.
– This lasts until cortical structure and medullary cavity are restored.
• Osteoblasts form new bone by producing osteoid.
∘ Derived from osteoprogenitor cells, under the influence of bone morphogenetic proteins
(BMPs).
∘ They produce alkaline phosphatase, which has a role in bone mineralisation.
• Osteoclasts are responsible for bone resorption.
∘ Derived from monocyte stem cells, similar to macrophages.
∘ They are large, multinucleate cells capable of phagocytosis.
• Osteocytes are osteoblasts that have become trapped within lacunae in bone matrix.
∘ They maintain bone matrix and contribute to calcium homeostasis.

General Principles

33

• Osteoid is the unmineralised, organic component of bone.
∘ Consists of proteins and ground substance made by osteoblasts.
∘ Type I collagen is the main protein; ground substance comprises chondroitin sulphate
and osteocalcin.

Primary bone healing
• This is healing without callus formation.
• Occurs if bone ends are directly apposed and fixed with absolute stability.
• Fracture haematoma is removed during surgery.
• The bone is ‘tricked’ into thinking it was never fractured.
• Inflammatory and proliferative phases of healing do not occur.
• Rather, it is a process of osteonal bone remodelling:
∘ Osteoclasts ‘drill’ across the fracture site from one cortex to the other.
∘ The tunnel allows blood vessels and osteoblasts to cross the fracture.
∘ This establishes new Haversian systems and normal bone architecture.
Secondary bone healing
• This is healing by callus formation.
• Occurs if fragments are not rigidly fixed, or if a gap exists between bone ends.
• It cannot occur if there is no fracture haematoma.
Complications of fractures
• Delayed union
• Non-union
• Malunion – rotation, angulation, shortening
• Infection
• Avascular necrosis (AVN)
• Damage to adjacent structures.

Bone graft healing
• Bone graft materials may be:
∘ Biological
– Autograft, allograft, xenograft
∘ Engineered biological
– Growth factors, recombinant BMPs, stem cells, platelet-rich plasma concentrate
(PRPC)
∘ Synthetic
– Metals, ceramics, polymers.
• Gold standard is autologous bone graft, usually harvested from iliac crest.
• Autologous bone grafts heal by these mechanisms:

Incorporation
• This is adherence of the graft to the host tissue.
• Incorporation is maximised in immobilised, well-vascularised tissue.

34

Chapter 1

Osseoconduction
• Bone graft acts as a scaffold along which vessels and osteoprogenitor cells travel.
• Old bone is resorbed as new is deposited.
• Also known as creeping substitution.
Osseoinduction
• This is differentiation of mesenchymal cells within local tissue into osteocytes.
• Osteoclasts, osteoblasts and osteocytes within bone graft are not capable of mitosis.
• Increased numbers of these cells within bone graft are derived from the recipient site.
• Osseoinduction is controlled by BMPs.
Osteogenesis
• This is formation of new bone by surviving cells within the bone graft.
• It is how most new bone is formed in vascularised bone grafts (bone flaps).
• Vascularised bone grafts incorporate more rapidly this way, without creeping substitution.
• Not much osteogenesis occurs in non-vascularised bone grafts.

Survival of bone grafts
• Factors influencing survival of bone grafts include:
1 Systemic factors
2 Intrinsic graft factors
3 Factors relating to the placement of the graft.

Systemic factors
• Age
• Nutrition
• Immunosuppression
• Drugs
• Diabetes
• Smoking
• Obesity.
Intrinsic graft factors
• Grafts with periosteum included undergo less resorption than those without.
• Membranous bone undergoes less resorption than endochondral bone when used as onlay
grafts in the face.
• Cancellous grafts are more easily revascularised than cortical grafts.
Graft placement factors
Orthotopic or heterotopic placement
• Orthotopic – graft is placed into a position normally occupied by bone.
• Heterotopic – graft is placed into a position not normally occupied by bone.
• Grafts in an orthotopic position are less prone to resorption.

General Principles

35

Quality of the recipient bed
• Radiotherapy, scarring and infection adversely affect graft survival.
Graft fixation
• Rigidly fixed grafts survive better than mobile ones.
Site of graft placement
• Grafts survive better in areas in which bone is normally laid down (depository sites).
∘ Includes areas such as zygoma and mandible in children.

Cartilage healing and cartilage grafts
Cartilage structure
• Derived from condensed mesenchyme.
• Differentiates into chondroblasts that secrete extracellular matrix.
• Chondroblasts eventually get trapped in lacunae within the matrix and become chondrocytes.
• The matrix contains type II collagen, elastin and ground substance (GAGs).
• Cartilage is classified according to the relative proportions of these three matrix components into:
1 Hyaline cartilage
2 Fibrocartilage
3 Elastic cartilage.
• Its molecular structure confers tensile strength and elasticity.
• This facilitates absorption and distribution of mechanical loads.
• Large amounts of water within the matrix help maintain its three-dimensional structure.
• Its viscoelastic properties allow it to resume its original shape after deformation.

Cartilage nutrition
• Cartilage has no intrinsic blood, nerve, or lymph supply.
• Its water content is important because it relies on diffusion of nutrients and oxygen
through the matrix.

Cartilage healing
• Chondrocytes show little reparative ability; healing is typically fibrous.
• Lack of blood supply makes healing very slow.

Cartilage grafts
1 Autografts
2 Allografts
3 Xenografts.

36

Chapter 1

Autografts
• These are the gold standard.
• Used for nose, ear and craniofacial reconstruction.
• Donor sites include:
∘ Ear conchal bowl
∘ Nasal septum
∘ Costal cartilage.
• Most cartilage grows from the deep layer of perichondrial connective tissue.
∘ Inclusion of perichondrium is therefore thought to be important for continued growth
of cartilage after grafting.
• Cartilage has a low metabolic rate; it is resistant to the ischaemia associated with grafting.
• Compared with bone graft, it is more easily shaped and undergoes less resorption.
• One major drawback is warping.
∘ This is a tendency to deform under mechanical stress over several days.
• Gillies in 1920 noted that cartilage carved on one side would curve towards the opposite
side.
• This was originally thought to be due to tension in the perichondrium, but its removal did
nothing to prevent warping.
• Experiments subsequently showed the outer layer of cartilage acted as a ‘taut skin’, preventing it from expanding on the intact side.
∘ This phenomenon, known as Gibson’s principle, has practical use in prominent ear correction by the anterior scoring method.
• Warping is most noticeable in the nasal dorsum due to thin overlying skin.
• The naturally straight segment of the 10th or 11th rib shows minimal tendency to warp.
• Most warping of cartilage grafts occurs within 60 minutes of transplantation, and continues for at least 4 weeks.
• For this reason, delaying implantation for at least 30 minutes after harvest is advocated.
∘ This allows the cartilage to assume its eventual curvature prior to fixation.
Allografts
• Cartilage allografts are generally unsuccessful in plastic surgery.
• The matrix is non-immunogenic and protects chondrocytes from circulating lymphocytes.
• However, once the matrix breaks down, chondrocytes are exposed and undergo rejection.
• This explains the slow but steady resorption of cartilage allografts.
Xenografts
• These remain immunogenic even after processing.
• They are therefore unsuitable for human implantation.

Nerve healing and nerve grafts
Nerve anatomy and function
• Nerve cells (neurons) consist of a cell body from which nerve fibres project.
• Outgoing impulses are carried by nerve fibres called axons.

General Principles

•
•
•
•
•
•
•
•
•
•
•

37

Impulses are received either on the cell body or nerve fibres called dendrites.
Endoneurium surrounds individual nerve fibres or axons.
Perineurium surrounds groups of nerve fibres (fascicles).
Intraneural epineurium contains blood vessels and surrounds perineurium.
The outer epineurium surrounds groups of fascicles to form a peripheral nerve.
Schwann cells produce the multilaminated myelin sheath of myelinated nerves.
Unmyelinated nerves are ensheathed by a Schwann cell-derived double basement
membrane.
Schwann cells of myelinated nerves abut at nodes of Ranvier.
Nerve conduction involves passage of an action potential along a nerve.
The impulse in myelinated nerves jumps between adjacent nodes of Ranvier.
∘ Known as saltatory conduction.
Nerve fibres are classified based on their diameter:

Group A
• Myelinated, large-diameter, high-conduction velocity nerves.
∘ Group A-α fibres: motor and proprioception.
∘ Group A-β fibres: pressure and proprioception.
∘ Group A-γ fibres: motor to muscle spindles.
∘ Group A-δ fibres: pain, touch, temperature.
Group B
• Myelinated, small-diameter, low-velocity fibres.
• Found in preganglionic autonomic nerves.
Group C
• Unmyelinated, small-diameter, low-velocity fibres, found in:
∘ Postganglionic autonomic nerves
• Dorsal root nerves for pain, temperature, touch, pressure and itch.

Medical Research Council grading of nerve function
• The MRC have recommended the following grading of nerve function:

Motor function
M0
M1
M2
M3
M4
M5

No contraction
Flicker
Movement with gravity eliminated
Movement against gravity
Movement against resistance
Normal

Sensory function
S0
S1
S1+
S2
S2+
S3
S3+
S4

No sensation
Pain (deep)
Pain (superficial)
Pain and some touch
S2 with over-response
S2 without over-response
Imperfect two-point discrimination
Normal

38

Chapter 1

Injury
• After nerve transection, degeneration occurs proximally to the nearest node of Ranvier.
• Distally, nerves undergo Wallerian degeneration.
• This process was described by Waller in 1850 and consists of:
∘ Degeneration of axons and myelin.
– Phagocytosed by macrophages and Schwann cells.
∘ Remaining basement membranes form endoneurial tubes that have a bandlike appearance on electron microscopy.
– Known as bands of Büngner.
– Important for guiding regenerating axons to their targets.
• Neurotropism is selective, directional growth of fibres towards end organs.
∘ Mediated by nerve growth factors and cell–cell interactions:
1 The proximal axon sprouts many new daughter axons, forming a growth cone.
2 Fibres growing in an inappropriate direction atrophy.
3 Those growing in the correct direction survive.
• Neurotrophism is non-selective, non-directional growth of nerve fibres.
• Neurotrophic factors are almost all produced by Schwann cells:
∘ Growth factors
– Nerve growth factor, ciliary neurotrophic factor, insulin-like growth factor.
∘ Extracellular matrix components
– Fibronectin, laminin, neural cell adhesion molecule, N-cadherin.

Classification of nerve injury
• Degree of nerve injury has been classified by Seddon and Sunderland.
• Seddon classification:
1 Neurapraxia
2 Axonotmesis
3 Neurotmesis.
• Sunderland expanded this classification:
First-degree injury
• Axon remains in continuity although conduction is impaired.
• Recovery should be complete.
Second-degree injury
• Axonal injury occurs and the segment of nerve distal to the site of damage undergoes
Wallerian degeneration.
• All connective tissue layers remain intact and recovery should be good.
Third-degree injury
• Axon and endoneurium are divided.
• Perineurium and epineurium remain intact.
• Recovery should be reasonable.

General Principles

39

Fourth-degree injury
• Complete division of all intraneural structures.
• Epineurium remains intact.
• Recovery of some function is expected.
• May result in a neuroma-in-continuity.
Fifth-degree injury
• Nerve trunk completely divided.
• Early surgical repair is mandatory for any recovery.
• Mackinnon added a sixth-degree injury to the classification.
∘ This is a mixed pattern nerve injury with segmental damage.
• Seddon’s neurapraxia equates to a Sunderland first-degree injury.
• Axonotmesis equates to a second-, third- or fourth-degree injury.
• Neurotmesis equates to a fifth-degree injury.

Nerve repair
• Nerve repair by direct approximation should be performed where possible.
• Nerve ends are trimmed and an epineurial repair under magnification with fine sutures
is done.
• Fascicles of nerve trunks should be aligned if possible.
• Repairs should not be under undue tension.
• Some authorities state primary repair should only be performed when a single 9/0 suture
is strong enough to appose the nerve ends.
• Clinical studies have not shown clear superiority of fascicular repair over epineurial repair.

Fascicular identification
• The following can aid fascicular matching during nerve repair.
Matching of anatomical structures
• Size and orientation of fascicles
• Distribution of vessels on the nerve’s surface.
Electrical stimulation
• Motor nerves respond to stimulation for up to 72 hours after division.
• Stimulation of the distal stump can differentiate motor from sensory fibres.
• Stimulation in a conscious patient can differentiate motor from sensory fibres in the proximal stump:
∘ Stimulation of sensory fibres produces sharp pain.
∘ Stimulation of motor fibres feels like a dull ache.
Knowledge of internal nerve topography
• The fascicular layout of many nerves is known and can be used to aid accurate repair.
• Ulnar nerve motor fascicles lie centrally between volar sensory branches from the palm
and dorsal sensory branches from the dorsal hand.

40

Chapter 1

Nerve grafts
• Required if primary repair not possible without undue tension.
• For large nerves, multiple cables of smaller donor nerves may be required to bridge the
defect.
• Tension across the repair can be reduced by mobilising the nerve proximally and distally,
and:
∘ Anterior transposition of the ulnar nerve at the elbow.
∘ Intratemporal dissection of the facial nerve.
• Nerve gaps can be bridged by autografts, allografts, or synthetic materials.
∘ Autologous nerve is the gold standard.

Composition
• Autologous tissues used to bridge nerve gaps include:
∘ Fresh nerve
∘ Freeze–thawed muscle
∘ Segments of vein.
• Allograft nerves require systemic immunosuppression to prevent rejection.
• Immunosuppression is withdrawn after Tinel’s sign has progressed into the distal nerve.
• Tacrolimus is the immunosuppressant of choice due to its neuroregenerative properties.
• Absorbable synthetic nerve tubes of polyglycolic acid have been trialled.
Autologous grafts
• Common sources of autologous grafts:
Sural nerve
• Passes behind lateral malleolus.
• Proximally, it divides into medial sural and peroneal communicating branches.
• Lengths up to 30–40 cm are available in adults.
• Can be harvested endoscopically.
Lateral antebrachial cutaneous nerve
• Lies adjacent to cephalic vein alongside ulnar border of brachioradialis.
• Lengths up to 8 cm are available.
• Harvest results in limited loss of sensation due to territory overlap with adjacent nerves.
Medial antebrachial cutaneous nerve
• Found in the groove between triceps and biceps, alongside basilic vein.
• Distally, divides into anterior and posterior branches.
• Posterior branch preserved if possible – supplies the resting part of elbow and forearm.
• Lengths up to 20 cm are available.
The terminal branch of the posterior interosseous nerve
• Useful for bridging small defects in small-diameter nerves.
• Located in the base of the fourth extensor compartment of the wrist.
• Only a relatively short length of nerve graft is available.

General Principles

41

Principles
• Both nerve ends are trimmed back to healthy tissue.
• Grafts are reversed to funnel regenerating axons distally.
• Place grafts on a healthy vascular bed, or transfer as a vascularised graft.
• Avoid tension on the graft.
• Stagger the level of repair between separate cables.
• Separate cables from each another as they bridge the defect.
• Proper sensory and motor alignment should be restored.

Tendon healing
Anatomy
• Tendons are composed of dense, metabolically active connective tissue.
• Collagen bundles are arranged in a regular spiralling fashion.
∘ Collagen is predominantly type I, with small amounts of types III and IV.
• Tendons contain few cells; those that are present include:
∘ Tenocytes
∘ Synovial cells
∘ Fibroblasts.
• Endotendon encloses tendon bundles.
∘ Continuous with perimysium proximally and periosteum distally.
• Epitenon is the outer layer of synovial tendons.
• Paratenon is a loose adventitial layer that surrounds extra-synovial tendons.
∘ These layers contain blood vessels.
• Flexor tendons receive blood supply from:
1 Musculotendinous junction
2 Bony insertion
3 Mesenteric vincular vessels.
• An avascular zone exists on the volar (frictional) surface of the tendon.
• Extensor tendon blood supply is similar, except that:
1 A long mesotenon exists within the synovial-lined extensor retinaculum.
2 There is no vincular supply.
• Over the dorsal wrist, extensor tendons are arranged into six synovial-lined compartments:
∘ 1st compartment: abductor pollicis longus, extensor pollicis brevis.
∘ 2nd compartment: extensor carpi radialis longus and brevis.
∘ 3rd compartment: extensor pollicis longus.
∘ 4th compartment: extensor indicis and extensor digitorum.
∘ 5th compartment: extensor digiti minimi.
∘ 6th compartment: extensor carpi ulnaris.

Mechanisms of tendon healing
Extrinsic healing
• Dependent on fibrous attachments forming between tendon sheath and tendon.

42

Chapter 1

• Historically believed to be the sole mechanism of tendon healing.
• Led to development of post-operative protocols that immobilised tendons in the mistaken
belief that this maximised tendon healing.

Intrinsic healing
• Dependent on:
∘ Blood flow through long and short vinculae.
∘ Diffusion of nutrients from synovial fluid.
• Lunborg showed tendons heal when wrapped in a semipermeable membrane and placed
in the knee joint of a rabbit.
∘ Enclosing the tendons in semipermeable membrane stimulates intrinsic healing as it
permits passage of nutrients, but not cells.
• Discovery of intrinsic healing led to early post-operative mobilisation (see Chapter 5,
‘Hand trauma’).

Phases of tendon healing
• Similar to those of wound healing.

Inflammation
• Inflammatory cells infiltrate the wound.
• Secrete growth factors that attract fibroblasts.
Proliferation
• Fibroblasts are responsible for tissue proliferation.
• They secrete type III collagen and GAGs.
• Collagen is initially arranged randomly; consequently, the tendon lacks strength.
Remodelling
• Begins approximately 3 weeks following tendon injury.
• Type III collagen is replaced by type I.
• The tendon remodels into an organised structure.
• Early motion limits fibrous attachments between tendon and sheath.
∘ It therefore promotes intrinsic healing at the expense of extrinsic healing.
∘ Mobilised tendons are stronger than immobilised tendons.

Transplantation
• Transplantation is transfer of tissue from one body location to another.
∘ Orthotopic transfers are transplants into an anatomically similar site.
∘ Heterotopic transfers are transplants into an anatomically different site.
• Transplant tissue types are classified as follows:
1 Autografts
∘ Transplantation within the same individual.
∘ Includes all flaps and grafts.
∘ Flaps carry intrinsic blood supply with them; grafts do not.

General Principles

43

2 Isografts
∘ Transplantation between genetically identical individuals.
3 Allografts
∘ Transplantation between different individuals of the same species.
∘ Also called homografts.
∘ Large burns can be temporarily covered with allograft skin.
4 Xenografts
∘ Transplantation from one species to another.
∘ Previously called heterografts.
∘ Porcine skin grafts can be used as temporary cover for burns.
∘ Implantable materials, e.g. Permacol and Strattice, are modified porcine xenografts.

Transplant immunology
History
• Gibson and Medawar were pioneers of transplant immunology in the 1940s and 1950s.
• They described the second set phenomenon, defined as ‘accelerated rejection of allogenic
tissue due to the presence of humoral antibodies from prior exposure to the same allogenic
source’.
• The first set reaction occurs when skin allograft is applied to an individual for the first
time.
• The first set reaction is characterised by:
1 During the first 1–3 days, allograft behaves in a fashion similar to autograft in that it
develops dilated capillaries with no blood flow.
2 Between 4 and 7 days, leukocytes and thrombi infiltrate the graft; punctate haemorrhages appear within its vessels.
3 Between 7 and 8 days, blood flow ceases and the skin graft necroses.
• The second set reaction occurs in patients who have been previously grafted with the same
allograft material.
• The second set reaction is characterised by:
1 Immediate hyperacute rejection.
2 The graft never undergoes any revascularisation, termed a ‘white graft’.

Immunology
• Rejection occurs when the host immune system recognises foreign antigens.
• ABO blood group antigens are potent barriers to transplantation.
∘ ABO matching is easily achieved but other antigens also mediate rejection.
• These antigens are encoded in the major histocompatibility complex (MHC).
∘ In humans, these are known as human leukocyte antigens (HLAs).
• HLAs of significance are six closely linked genes on the short arm of chromosome 6 and
are divided into two classes:
∘ Class I: HLA-A, -B and -C; found on all nucleated cells and platelets.
∘ Class II: HLA-DP, -DQ and -DR; found on APCs.
– APCs include monocytes, macrophages, dendritic cells (called Langerhans cells in
skin), B lymphocytes and activated T cells.
• HLA-A, -B and -DR are the most important mediators of tissue rejection.

44

Chapter 1

• HLAs on APCs can be recognised by T cells via two separate pathways:
1 Direct pathway
– Unique to transplantation.
– Recipient T cells recognise HLAs on donor APCs within transplanted tissue.
– Initiates a strong immune response.
– Thought to be the major route for initiating acute rejection.
2 Indirect pathway
– Physiological pathway activated in response to non-self antigens, e.g. viruses.
– Recipient T cells recognise donor HLAs after processing by recipient APCs.
• Host immune response is co-ordinated by T helper (Th ) cells.
∘ Activation of Th cells by direct or indirect pathways induces them to differentiate along
the Th 1 (cell-mediated response) or Th 2 (humoral response) route.
– Release of IL-12 from APCs favours Th 1 differentiation; IL-4 favours Th 2 differentiation.
• Th 1 cells release the cytokines IL-2, IFN-γ, TNF-α and TNF-β.
∘ These activate macrophages and natural killer (NK) cells that cause direct graft cell lysis.
– Known as delayed type hypersensitivity (DTH) reaction.
∘ Cytotoxic CD8 T cells are also stimulated to destroy allograft cells by inducing apoptosis
(Fas activation) and releasing lytic enzymes.
• Th 2 cells release interleukins, particularly IL-4.
∘ Stimulate B cells to mature into antibody-producing plasma cells.
∘ These antibodies stimulate tissue destruction by complement fixation, or by targeting
neutrophils, eosinophils, macrophages and NK cells to the graft.
• A combination of Th 1 and Th 2 responses occurs in most immune reactions.
• IL-2 is the principal T-cell growth factor.
∘ An important target for immunosuppressive drugs.
Hyperacute rejection
• Occurs within minutes.
• Pre-existing antibodies to the donor, e.g. anti-ABO blood group antibodies, activate complement.
• The allograft must be removed immediately to prevent systemic inflammatory response.
• Seen with some xenografts:
∘ Discordant transplantation occurs when natural antibodies between species are present,
e.g. pig to human.
∘ Concordant transplantation occurs when natural antibodies are not present, e.g. primate
to human.
Acute rejection
• Occurs after 1 week due to the delay in T-cell activation.
• May occur years after transplantation.
• Usually treated with a short course of high-dose corticosteroids.
• Recurrent episodes may lead to chronic rejection.

General Principles

45

Chronic rejection
• Poorly understood chronic inflammatory and immune response.
• Irreversible; treatments, other than re-transplantation, are ineffective.

Immunosuppression
• Subdivided into non-specific and specific modalities.
• Non-specific techniques of immunosuppresion:

Radiation
• Whole-body radiation removes mature lymphocytes; not used in humans.
• Localised lymphoid tissue irradiation is specifically targeted, e.g. thymus.
• Graft irradiation reduces antigenicity by destroying Langerhans cells in skin.
Drugs
• Three main groups of immunosuppressants:
1 Steroids, e.g. prednisolone
– Anti-inflammatory and immunosuppressive.
– Usually used in combination with other agents.
2 Cytotoxics, e.g. cyclophosphamide, methotrexate, mycophenolate mofetil, azathioprine.
– Interfere with DNA replication; kill proliferating lymphocytes.
3 Fungal or bacterial products, e.g. ciclosporin, tacrolimus, sirolimus.
– Ciclosporin and tacrolimus block calcineurin activation.
• Decrease production of IL-2 and subsequent T-cell activation.
– Sirolimus (or rapamycin) is a newer drug that blocks lymphocyte proliferation and
differentiation.
• It inhibits mammalian target of rapamycin (mTOR) protein.
Biological agents
• Anti-lymphocyte serum is made by injecting another species with lymphoid tissue from
the recipient.
• The resulting polyclonal anti-thymoglobulin (ATG) and anti-lymphocyte sera (ALS)
deplete recipient T cells.
• Specific techniques of immunosuppression involve monoclonal antibodies directed
towards specific antigens.
∘ Basiliximab prevents IL-2-mediated clonal expansion of activated lymphocytes.
∘ This is an area of intense research as new antibody targets are discovered.
Immunological tolerance
• Transplant research is focused on development of immunological tolerance.
• Tolerance is the state of immunologic acceptance or unresponsiveness of a recipient to
donor allograft or xenograft.
• Induction of tolerance allows transplantation without need for immunosuppression.

46

Chapter 1

Vascularised composite allotransplantation (VCA)
• VCA involves transplantation of various tissues such as skin, nerve, blood vessel, muscle
and bone from one human to another.
• Previously known as composite tissue allotransplantation (CTA).
• Examples pertinent to plastic surgery include limb and face transplantation.

History
• A hand transplant was performed in Ecuador in 1963, but was acutely rejected within a
few weeks.
• In 1997, the International Symposium on CTA was held in Louisville, Kentucky, to discuss
possible human hand allotransplantation.
∘ Concluded that it was appropriate to consider undertaking the procedure.
• The first successful hand transplant was performed in 1998 by an international surgical
team assembled in Lyon, France.
∘ This was repeated in 1999 by units in Louisville, USA and Guangzhou, China.
• Thus it became clear that modern immunosuppressive drugs could allow skin, muscle and
bone allotransplants to survive and function.
• This stimulated interest in face transplantation.
• Facial transplantation was shown to be technically possible by a microsurgical team in
India led by Abraham Thomas.
∘ In 1994 they reattached the face and scalp of a 9 year-old girl after it was avulsed by a
machine.
• In 2002, Peter Butler discussed the potential for face transplantation at the BAPS Winter
Meeting.
• A working party set up by the Royal College of Surgeons of England examined all aspects
of the proposed procedure.
∘ They reported in 2003 that further research was required before facial transplantation
could be performed.
• The Comité Consultatif National d’Ethique (CCNE) in France produced a report in 2004.
∘ They concluded that a partial face transplant involving the mouth–nose triangle could
be performed.
• The first successful partial face transplant was done in 2005 by a team based in Amiens,
France.
• The first full face transplant was done in Barcelona by a Spanish team in 2010.
• At the time of writing, the most extensive face transplant was performed in 2012 at the R
Adams Cowley Shock Trauma Center in Baltimore, Maryland.
∘ The transplant replaced almost everything from the coronal plane of the scalp to the
clavicles.
• The first British VCA was a right hand transplant performed by the UK Hand Transplant
Programme in Leeds on 27th December 2012.
Technical considerations
• Routine techniques of microsurgery and organ harvest, refined over many years.

General Principles

47

Biological considerations
• High rejection rates were anticipated due to the perceived high antigenicity of skin.
• This is not borne out in practice:
∘ Immunosuppressant regimes for VCAs are virtually identical to those for solid organ
transplantations.
∘ Most employ either basiliximab or ATG for induction therapy, and triple maintenance
therapy with tacrolimus, mycophenolate mofetil and prednisolone.
Ethical considerations
• Although VCAs enhance quality of life, they are not essential for life.
• Quality of life is a subjective judgement that varies between VCA recipients.
Psychological considerations
• These are at the forefront of VCA research.
• Transplantation may have unpredictable psychological effects:
∘ Anxiety
– Regarding the transplant, rejection, side effects of medication.
∘ Identity
– Integration of the VCA into body image, self-recognition.
∘ Adjustment
– Ability to adjust is not well predicted by the severity of disfigurement.
Consent
• Must be completed well in advance of a transplant.
∘ There is insufficient time once a suitable donor is identified.
Patient selection
• A comprehensive and coherent protocol is used to select suitable patients.
• Should address physical, psychological and social attributes of the recipient.

Tissue engineering
• Langer and Vacanti, considered the fathers of tissue engineering, define this term as ‘an
interdisciplinary field that applies the principles of engineering and life sciences toward the
development of biological substitutes that restore, maintain, or improve tissue function or
a whole organ’.
• The first tissue-engineered implant was a chondrocyte